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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
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Targeting KDM1B-dependent miR-215-AR-AGR2-axis promotes sensitivity to enzalutamide-resistant prostate cancer

Donge Tang1,2, Jiaxi He3, Yong Dai2

  • 1Research Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.

Cancer Gene Therapy
|April 15, 2021
PubMed

Insights

Histone demethylase KDM1B is upregulated in enzalutamide-resistant prostate cancer, driving tumor growth. Inhibiting KDM1B may overcome resistance by targeting the miR-215-KDM1B-AR-AGR2 pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Histone demethylases regulate gene transcription and are linked to cancer development.
  • Castrate-resistant prostate cancer (CRPC) often develops resistance to therapies like enzalutamide due to androgen receptor signaling.
  • The role of KDM1B in enzalutamide resistance and its regulatory mechanisms in prostate cancer are not well understood.

Purpose of the Study:

  • To investigate the role of KDM1B in enzalutamide-resistant prostate cancer.
  • To elucidate the regulatory mechanisms of KDM1B in this context.
  • To evaluate KDM1B inhibition as a therapeutic strategy against enzalutamide resistance.

Main Methods:

  • Analysis of KDM1B expression in prostate cancer tissues and correlation with progression and prognosis.
  • Investigation of the relationship between miR-215 and KDM1B in enzalutamide-resistant prostate cancer cells.
  • Assessment of the impact of KDM1B inhibition on tumor growth and response to enzalutamide therapy, focusing on AGR2 suppression.

Main Results:

  • KDM1B is upregulated in prostate cancer and correlates with poor prognosis.
  • Downregulation of miR-215 is associated with KDM1B overexpression in enzalutamide-resistant cells.
  • KDM1B promotes androgen receptor-dependent AGR2 transcription, affecting therapy sensitivity.
  • Inhibition of KDM1B suppresses tumor growth and enhances enzalutamide efficacy via AGR2 suppression.

Conclusions:

  • KDM1B plays a critical role in enzalutamide resistance in prostate cancer.
  • The miR-215-KDM1B-AR-AGR2 signaling axis is a key driver of resistance.
  • Targeting KDM1B presents a promising therapeutic approach to overcome enzalutamide resistance in prostate cancer.

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